In the field of hematological malignancies, myeloid neoplasms represent a diverse set of diseases including myelodysplastic syndromes, myeloproliferative neoplasms, and acute myeloid leukemia, predominantly affecting older adults. The foundation of these diseases lies in the faulty epigenetic regulation of transcriptional programs essential for the differentiation and self-renewal of hematopoietic cells. Disruptions in DNA methylation and histone modification pathways can initiate clonal hematopoiesis, leading to the development and advancement of these malignancies. Despite recent strides in molecular sequencing and epigenetic pathway analysis, current epigenetic therapies have not yet demonstrated curative effects. Persistent issues like tumor heterogeneity, resistance mechanisms, and the evolution of cancer clones complicate treatment efforts by altering the oncogenic landscape, thus enhancing oncogene activity while suppressing tumor suppressor genes.
This Research Topic aims to delve into the complex interplay of genetic and epigenetic anomalies contributing to myeloid neoplasms, with an emphasis on identifying and understanding the molecular mechanisms at play. More specifically, it seeks to elucidate how alterations in DNA methylation and histone modifications contribute to the pathogenesis of these diseases, the role of mutational processes in tumorigenesis, and how these processes contribute to resistance and disease progression. Ultimately, the objective is to harness these insights to improve the management and treatment protocols for myeloid neoplasms, transforming these findings into innovative therapeutic strategies.
To advance our understanding of these complex diseases, this topic is delineated within the realms of molecular and cellular mechanisms and their therapeutic implications. We invite contributions that focus on:
-Epigenetic dysregulation in myeloid neoplasms, including specific mutations in DNA methylation and posttranslational histone modifications.
-Genomic alterations driving tumorigenesis in myeloid neoplasms, such as variance in mutations, genomic rearrangements, and their impacts on tumor heterogeneity and clonal evolution.
-Novel therapeutic approaches targeting epigenetic dysregulation, exploration of personalized medicine strategies, and the integration of clinical applications.
-Diagnostic features that characterize particular phenotypes or variants of myeloid neoplasms during their progression or evolution.
Through the incorporation of original research, reviews, case studies, and methodological innovations, this topic seeks to broaden the horizon of epigenetic research in myeloid malignancies from basic studies to clinical applications.
Keywords:
Hematopoeitic stem cell, epigenome, myeloid neoplasms, DNA methylation pathway, histone modification, nucleosome, gene expression, mutations, methylome, gene rearranegments, epigenetic modifiers
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
In the field of hematological malignancies, myeloid neoplasms represent a diverse set of diseases including myelodysplastic syndromes, myeloproliferative neoplasms, and acute myeloid leukemia, predominantly affecting older adults. The foundation of these diseases lies in the faulty epigenetic regulation of transcriptional programs essential for the differentiation and self-renewal of hematopoietic cells. Disruptions in DNA methylation and histone modification pathways can initiate clonal hematopoiesis, leading to the development and advancement of these malignancies. Despite recent strides in molecular sequencing and epigenetic pathway analysis, current epigenetic therapies have not yet demonstrated curative effects. Persistent issues like tumor heterogeneity, resistance mechanisms, and the evolution of cancer clones complicate treatment efforts by altering the oncogenic landscape, thus enhancing oncogene activity while suppressing tumor suppressor genes.
This Research Topic aims to delve into the complex interplay of genetic and epigenetic anomalies contributing to myeloid neoplasms, with an emphasis on identifying and understanding the molecular mechanisms at play. More specifically, it seeks to elucidate how alterations in DNA methylation and histone modifications contribute to the pathogenesis of these diseases, the role of mutational processes in tumorigenesis, and how these processes contribute to resistance and disease progression. Ultimately, the objective is to harness these insights to improve the management and treatment protocols for myeloid neoplasms, transforming these findings into innovative therapeutic strategies.
To advance our understanding of these complex diseases, this topic is delineated within the realms of molecular and cellular mechanisms and their therapeutic implications. We invite contributions that focus on:
-Epigenetic dysregulation in myeloid neoplasms, including specific mutations in DNA methylation and posttranslational histone modifications.
-Genomic alterations driving tumorigenesis in myeloid neoplasms, such as variance in mutations, genomic rearrangements, and their impacts on tumor heterogeneity and clonal evolution.
-Novel therapeutic approaches targeting epigenetic dysregulation, exploration of personalized medicine strategies, and the integration of clinical applications.
-Diagnostic features that characterize particular phenotypes or variants of myeloid neoplasms during their progression or evolution.
Through the incorporation of original research, reviews, case studies, and methodological innovations, this topic seeks to broaden the horizon of epigenetic research in myeloid malignancies from basic studies to clinical applications.
Keywords:
Hematopoeitic stem cell, epigenome, myeloid neoplasms, DNA methylation pathway, histone modification, nucleosome, gene expression, mutations, methylome, gene rearranegments, epigenetic modifiers
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.